Perisomatic GABA release and thalamocortical integration onto neocortical excitatory cells are regulated by neuromodulators (Neuron, 2008, 58:911-924)

報告日期: 2008/12/19
報告時間: 15:10/16:00
報告學生: 林宏國
講評老師: 許桂森
附件下載:

http://basicmed.med.ncku.edu.tw/admin/up_img/971219-1.pdf

Perisomatic GABA Release and Thalamocortical Integration onto Neocortical Excitatory Cells Are Regulated by Neuromodulators

Illya Kruglikov and Bernardo Rudy        

Neuron 58: 911–924, 2008

 

Speaker: Hong-Guo Lin (林宏國)

Commentator: Kuei-Sen, Hsu, Ph.D (許桂森 老師)

Date: 12/19 15:10 – 16:00

 

Abstract

The neocortex is the target of extensive ascending projections releasing neurotransmitters such as acetylcholine (ACh), serotonin (5-HT), dopamine, and noradrenaline and is exposed to activity-dependent levels of substances such as adenosine and GABA. These neuromodulators have a profound influence on the function of the cerebral cortex due to their effects on the excitability and synaptic properties of neocortical neurons. However, little is known about their effects on GABA release from specific interneuron (IN) types because different interneuron classes control specific aspects of excitatory cell function. Therefore, the authors screened for agents that modulate the inhibitory postsynaptic currents (IPSCs) evoked in layer 5 pyramidal cells (PCs) by extracellular stimulation using an assay biased toward detecting modulation of GABA release from fast-spiking (FS) cells, the most prevalent interneuron subtype in neocortex. They found that GABA release from FS cells is robustly inhibited following activation of muscarinic, serotonin, adenosine, and GABAB receptors. Furthermore, they used FS-to-PC paired recordings to confirm that the modulations occur at FS cell synapses. The results show that the powerful suppression of feedforward inhibition facilitates thalamocortical (TC) excitation of the cortex while activation of muscarinic receptors. They demonstrated that cholinergic action facilitates thalamocortical excitation of primary somatosensory cortex primarily by reducing feedforward inhibition. This effect was complemented by a nicotinic-mediated increase in the TC drive onto thalamo-recipient excitatory cells (ECs) as well as the muscarinic-mediated increase in the excitability of these cells.

 

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